Tropospheric Ozone:
Formation, Impacts and Regional Transport
Introduction
Ozone is an oxidant present in both the stratospheric level and the tropospheric level of the
earth=s atmosphere. It is produced by a photochemical reaction, meaning that the role of solar
radiation is essential in driving the chemistry of its formation. Ozone in the stratosphere occurs
naturally and is necessary for the protection of the earth from harmful ultraviolet solar radiation.
However, the excessive amounts of ozone in the troposphere result primarily from pollution, mostly
from anthropogenic sources, and can have harmful effects on human health and the environment and
vegetation.
Tropospheric or ground-level air pollution, also known as smog, has been a problem for
centuries with the burning of wood and, in the industrial era, coal. It originally was associated with
high concentrations of sulfur dioxide and soot particles and was dubbed ALondon Smog@ because of
a severe episode there in 1952. In the 1940=s a different kind of smog B photochemical smog B was
discovered in the Los Angeles area. Tropospheric ozone is the primary component of photochemical
smog. (Finlayson-Pitts and Pitts, 1997).
Ozone has historically been regarded as the principal urban and regional air quality problem
in the United States (Meng, et. al., 1997), and studies to determine the extent of its harmful effects
on both humans and on the environment have been ongoing for decades. Because of the health
concerns, ozone has been regulated by the U.S. Environmental Protection Agency under the Clean
Air Act since 1971. (CAA, Section 7511). However, ozone is not an emitted pollutant and is
instead formed in the atmosphere from other pollutants. Therefore, its regulation has focused on
controlling the emissions of its precursors that contribute to its synthesis.
Major sources of ozone precursors are coal-fired utilities, many of which are located in the
Midwestern United States. Recently, disputes between regions over emerging evidence of the longdistance transport of ozone across states has prompted the EPA and state regulatory agencies to begin
addressing the transport problem through cooperative efforts.
Formation of Ozone
The process by which ozone (O3) is created involves a series of complex photochemically
initiated reactions in the atmosphere involving nitrogen oxides (NOx), reactive hydrocarbons, and
oxygen (O2). Solar radiation wavelengths of at least 290 nm are required for inducing photochemical
reactions. (Finlayson-Pitts, 1997). A simplified version of this process is described as follows:
First, a photochemical reaction occurs by which NO2 is disassociated to produce NO and
atomic oxygen:
NO2  hv (  420 nm)  NO  O
The atomic oxygen reacts with atmospheric oxygen and with M, an energy-absorbing third
body, to produce ozone:
O2  O  M  O3  M
Finally, NO reacts with O3 to regenerate NO2 and, in the process, ozone is consumed.
O3  NO  NO2  O2
Under normal conditions and in the absence of competing reactants in the atmosphere, this
cycle would have no net effect. The ambient NO and NO2 concentrations would not change and O3
and NO would be formed and destroyed in equal quantities. However, this cycle is disrupted when
hydrocarbons are present because they are highly reactive with the oxygen or ozone atoms produced.
Hydrocarbons that react with O2 produce hydrocarbon free radicals (RO2), which can further react
with NO2, O2, O3 and other hydrocarbons to form more photochemical pollutants. (Stoker and
Seager, 1975).
The free radicals that affect ozone are those that react very rapidly with NO to produce NO2.
NO  RO2  NO2  RO
When this occurs, the cycle becomes unbalanced because NO is converted into NO2 faster
than NO2 is disassociated into NO and O. The major consequence of this reaction is that, with NO
removed from the cycle, the normal mechanism for O3 removal has been eliminated and the
concentration of O3 in the air increases. (Stoker and Seager, 1975).
Sources of Ozone Precursors
Examining the process of ozone formation demonstrates that the two major precursors of
ozone are nitrogen oxides and hydrocarbons. Although NOx and hydrocarbons are emitted into the
atmosphere from natural sources, the amounts causing air quality deterioration are produced by
anthropogenic sources. NOx are emitted from stationary sources through the combustion of fossil
fuels. Power plants account for most of those emissions, followed by other industries, and
commercial and home heating sources. Hydrocarbon emissions, on the other hand, result primarily
from industrial processing and the evaporation of solvents, such as those in paints, varnishes,
lacquers, coatings and similar products. Nevertheless, the major anthropogenic source of both of
these pollutants is the internal combustion engine used in automobiles and trucks. The EPA
estimates that motor vehicles are responsible for 37% of the anthropogenic emissions of
hydrocarbons and 49% of nitrogen oxides. (EPA,1997). Given these major sources of ozone
precursors, it is not surprising that high ozone levels are most frequently experienced in urban and
more populous areas where most industry and automobile traffic are located.
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Another component essential to the formation of ozone is heat energy from the sun. Because
of this need, there are significant variations in ozone concentrations during the course of a day
depending on the amount of sunlight. Ozone levels are generally lowest in the morning hours,
accumulating through midday, and decreasing rapidly after sunset and the time of day. (Christiani,
1993). Below is a graph of a typical day in an urban area (in this case Los Angeles) showing more
specifically the pattern of emissions of NOx and hydrocarbons and the formation of ozone related to
the time of day and the presence of sunlight.
1.
2.
3.
4.
5.
6.
7.
Before daylight, NO, NO2 and hydrocarbon levels remain fairly stable. As
human activity increases, NO peaks at around 6:00 to7:00 a.m., largely due to
the early morning rush hour automobile traffic.
Hydrocarbons follow a similar pattern as they are also emitted from the
automobiles, but peak at a later time.
As the sun rises, NO2 levels increase as NO reacts with O3.
NO begins to decrease at around 7:00 a.m. as it reacts with free radicals
produced by increasing hydrocarbons, producing more NO2.
NO2 photochemically disassociates, producing more O, and the O combines
with O2 to create more O3.
As the NO decreases and consumes less O3, levels of O3 increase, peaking
between 12:00 and 3:00 p.m.
As the solar intensity decreases, and automobile traffic increases at about
5:00 to 8:00 p.m. with the evening rush hour, the concentration of NO goes
up, and begins to consume the O3 that has built up during the day.
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This cycle then begins again the next day and repeats daily in a typical urban area. In many
other areas of the country, this ozone pattern is also dependent on the seasons. In those areas, higher
concentrations of ozone are most often observed in the summertime when the sunlight is most
intense and temperatures are highest. (NESCAUM, 1997).
Impacts of Ozone on Public Health and the EPA Standards
Ozone is a lung irritant that affects the respiratory tract and can be especially harmful to
sensitive populations, such as children and individuals with asthma. (Weisel, et. al., 1995).
Scientific studies of the impacts on humans have revealed a causal relationship between ozone
exposure and irritation of the airways leading to inflammation, increased permeability in lung tissue
and the destruction of pulmonary cells, and decreased lung function. (Spengler, 1993). There has also
been a relationship established between ozone levels and emergency room visits in the Northeast due
to respiratory-related problems. (Weisel, et. al.,1995). Exercising individuals typically experience
airway inflammation and hyperreactivity, decreased athletic performance, increased cough, altered
tracheobronchial clearance and increased permeability of the lung lining, especially during extended
exposures. (Leikauf, 1995). Evidence is emerging that ozone possibly impacts the immune system
defenses, making people more susceptible to respiratory illnesses, including bronchitis and
pneumonia. (Jakab, et. al., 1995).
The severity of the impacts seems to vary with the concentrations of ozone and the length of
exposure, i.e. intermittent or continuous. Intermittent acute exposures to ambient ozone result in
reversible changes in lung function and respiratory symptoms. Elevated levels of daily ozone (peak
hour) are associated with restricted activity, asthma symptoms and respiratory admissions to
hospitals. (Spengler, 1993).
There has recently been more concern about long-term exposures to ozone of a chronic lowlevel nature, which may result in permanent loss of lung function and an increase in associated
disease. (Last, et. al. 1994). Also, mixtures of ozone and other pollutants, such as NO2, have caused
pulmonary fibrosis and death in chronically exposed laboratory rats, demonstrating a response
greater than that to either ozone or NO2 alone. (Last, et. al. 1994). Two time-series studies have
associated changes in daily mortality with ozone and other pollutants in Los Angeles and New York
City. (Spengler, 1993).
The Clean Air Act regulates certain harmful pollutants by requiring the EPA to impose
National Ambient Air Quality Standards (or NAAQS) for those pollutants. Under the EPA must
promulgate two sets of standards: a primary standard sufficient to protect human health with an
adequate margin of safety, and a secondary standard to protect the environment, including plants,
animals, ecosystems, and visibility.
Ozone is one of the six criteria pollutants regulated under the Clean Air Act. Until recently,
both the primary and secondary ambient air quality standard for ozone was set at 0.12 parts per
million (ppm) for one hour, not to be exceeded more than once per year. To determine whether the
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standard is being met, ground-level ozone concentrations are measured continuously by monitoring
devices and hourly averages are calculated. Any areas in which average hourly ozone levels exceeded
0.12 ppm more that once per year are classified as Aozone nonattainment areas.@ In 1992, an
estimated 140 million people lived in ozone nonattainment areas. (Koenig, 1995)
Other countries have set various 1-hour ozone air quality standards or guidelines as well,
many of which are below 0.12 ppm. Canada has set a standard of 0.082 ppm, Japan, 0.06 ppm, and
the World Health Organization (WHO) for Europe, 0.075 - 0.10 ppm. (Weisel, et. al., 1995) Last
year, on September 16, 1997, after a lengthy scientific review process, the EPA lowered the standard
for ozone to 0.08 ppm and is replacing the 1-hour averages with a new 8-hour average to protect
against longer exposure periods. The EPA also replaced the previous secondary standard with an
identical standard to the primary standard.
Many environmentalists and public health advocates were pleased when the EPA lowered the
standard for ozone last year. Nevertheless, others question whether the 0.08 ppm standard averaged
over 8 hours is sufficient to protect the public health, especially that of children, asthmatics and
individuals that exercise frequently outdoors. In determining the effectiveness of the EPA standards
in protecting the public health, it is interesting to examine some of the studies conducted on the
health impacts of ozone relative to the EPA standards. Many of these studies were performed before
the EPA changed the standard and thus reference the 0.12 levels. However, because in many urban
areas ozone levels continue to exceed even the 0.12 ppm, these impacts are still very significant.
Research on the Impacts of Ozone on Human Health
There is a complex set of variables involved in the research of ozone=s adverse health effects
and different studies use different combinations of these variables. For example, adverse human
health effects, such as pulmonary function, can be measured by forced vital capacity (FVC), the
forced expiratory volume in the first second (FEV1), and/or peak expiratory flow rate (PEFR). Other
testing methods can reveal more localized effects, such as tests on lavage fluid, a saline solution used
to rinse the lungs and airways of subjects after exposure, or biopsies of tissue samples. Researchers
can conduct epidemiological studies, in which symptoms are recorded in diaries and through followup examinations while subjects perform functions in the natural environment, or controlled studies
conducted in laboratories. Lastly, different studies use alternative concentrations of ozone (estimated
peak daily ozone levels, average 24-hour levels, or levels averaged over a shorter time period) and
for varying lengths of exposure.
Several clinical and epidemiological studies have documented significant decrements in
pulmonary airflow in individuals exposed levels of ozone at or below the level of 0.12 ppm ozone.
(Leikauf, et. al., 1995). For example, earlier this year, a two-year study was published by researchers
at Brigham and Women=s Hospital and the Harvard School of Public Health which showed that
ozone levels common to non-urban parts of the U.S. were associated with decreases in lung function
in adult hikers in New Hampshire. The study evaluated the effects of ozone and other air pollutants
on the lung function of 530 nonsmokers hiking on New Hampshire=s Mount Washington over the
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course of two summers. The hikers ranged from age 18 to 64 and hiked an average of eight hours a
day. During this time they were exposed to ozone levels of 0.021 to 0.074 ppm per hour. The overall
average exposure was 0.04 ppm. The researchers measured the hikers FEV and FVC before and
after their hikes. They found that a 0.05 ppm increase in ozone concentration was associated with
decreased lung function over the course of the hike: an average 2.6% decline in FEV and a 2.2%
decline in FVC. More significantly, the researchers found that hikers with a history of asthma or
wheezing had an even greater decline: their ozone related changes were approximately four times
greater that the other subjects. (Korrick, et. al., 1998).
In general, ozone-associated changes in pulmonary function are greater in natural rather than
in controlled exposure settings. Although it is hypothesized that synergism or interaction with other
with other uncontrolled environmental factors play a role in this finding, the explanation for this
discrepancy continues to be unknown. (Korrick, et. al., 1998). However, the significance of the
findings of the New Hampshire study is the potential of negative health impacts of relatively low
levels of air pollutants, not only among residents of urban and industrial regions, but also among
individuals engaged in outdoor recreation in wilderness areas.
As demonstrated by the New Hampshire study, asthmatics have been shown to be more
sensitive to ozone levels than Ahealthy@ individuals. Dr. Jane Koenig reviewed recent research of
ozone exposure in asthmatics compared to non-asthmatics. (Koenig, 1995). In one study, conducted
by Dr. Koenig herself, ten asthmatic and eight nonasthmatic subjects participated. All were exposed
to clean air, air containing 0.12 ppm, and air containing 0.24 ppm ozone through a head dome
exposure system for 90 minutes during intermittent or moderate exercise. After exposure, bronchial
lavage tests revealed increased white blood cells from subjects with asthma immediately after
exposure to 0.24 ppm ozone and then again 24 hours after the exposure, indicating an inflammatory
response to ambient levels of ozone inhalation. There was also an increase in the epithelial cells in
the lining of the lungs and airways immediately after the exposure. No similar changes were seen in
the nonasthmatic subjects. The researchers concluded that asthmatic individuals are more susceptible
to acute inflammatory effects produced by low levels of ozone than the nonasthmatic individuals.
(Koenig, et. al, 1995).
Whereas this was a controlled experiment, the number of respiratory symptoms reported by
asthmatics increases in non-controlled environments on days when the ozone concentrations are
high. (Koenig, et. al., 1995) This is especially true for children, for which asthma is the number one
chronic disease. The number of children with asthma in the United States increased by 79% between
1982 and 1993. (NESCAUM, 1997). Whereas it has not yet been proven that ozone exposure causes
childhood asthma, it does initiate and aggravate asthmatic attacks in children, as well as adults,
already suffering from the disease. More recent research is being conducted to determine ozone=s
role in initiating or promoting asthmatic attacks. (Weisel, et. al., 1995).
A study was performed on 67 mildly asthmatic children ages 5 to 13 living in a 5 kilometer
radius in the metropolitan area of Mexico City. The area where the children lived was exposed
frequently to intermittently high ozone levels. For the study, the parents were instructed to document
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respiratory symptoms and the use of bronchodilators and other medications in daily diaries during
three study periods lasting several weeks over the course of one year. They were also asked to bring
the children in for a clinical exam at the end of each week. The researchers obtained measurements
at a local pollution-monitoring station to determine daily levels of ozone and other pollutants. During
the study period, maximum daily 1-hour ozone levels ranged from 0.04 to 0.39 ppm. The findings
revealed a positive association between daily reporting of respiratory symptoms and ozone
concentrations. On days when the concentrations exceeded 0.17 ppm, the prevalence of respiratory
symptomsCincluding the presence of cough, phlegm, and lower respiratory tract illness (LRI) B was
significantly higher than on days when ozone levels were below 0.12 ppm. Using statistical analysis,
they determined that an increase of .05 ppm in the daily 1-hour maximum O3 ambient concentrations
led to an 11% increase in LRI symptoms, a 29% increase in phlegm, and a 10% increase in cough on
the same day. They also determined a 3% increase in the use of broncholdilators.
Even healthy children with no underlying pulmonary diseases are at risk for adverse health
effects associated with ozone. (White, et. al. 1995) The reasons for this increased risk over adults are
twofold. First, children are more likely to spend increased amounts of time outdoors during summer
months when ozone levels are higher. Second, their lungs are more vulnerable because they are in
the development stages. Moreover, increased attention is being drawn to the disproportionate risks of
ozone exposure associated with the children of racial/ethnic minorities with low incomes in the
United States. These children are more likely to reside in urban areas and therefore may be exposed
to ozone levels that exceed the national ambient air quality standards. (White, et. al , 1995).
Impacts on Vegetation and Forests
In addition to human health impacts, ozone has also been found to significantly harm the
environment. It interferes with the ability of plants to produce and store food, making them more
susceptible to disease, insects, other pollutants, and harsh weather. (EPA, 1997). Exposure to ozone
also causes visible effects of ozone injury to plants such as bleached or light flecks or stipples (small
clusters of dead cells) on the upper surface of leaves. Mature leaves are the most easily damaged.
(Wall and Strong, 1985).
Ozone is responsible for 500 million dollars in reduced crop production in the United States
each year. (EPA, 1997). Growth and yield reductions result primarily from reduced photosynthesis
and transport of carbohydrates within plants. The National Crop Loss Assessment Program
performed an eight year study in which crops were grown in the field either in air filtered to assume
background ozone concentrations, ambient air or air to which extra ozone had been added. From its
studies, it estimated yield reductions for different types of crops. Corn, when exposed to a seasonal
average seven-hour mean ozone concentration of .04 ppm ozone, was estimated to experience 0 to
1.4% reduction in yield, but wheat could experience 0 to 29%. At .06 ppm, yield losses for corn
could be .3 to 5.1% and for wheat, .9 to 51%. The range of yield reductions indicated differences
among varieties. (OTA, 1988).
A study of germinated pea seedlings fumigated with ozone demonstrates the relationship of
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ozone and plant responses. Ethylene is a substance is normally produced by all plants and interacts
with other plant grown substances to coordinate developmental processes. When plants are exposed
to environmental stresses, they respond by releasing larger amounts of ethylene, referred to as stress
ethylene. One set of seedlings was fumigated at levels of 50 to 150 ppbv (parts per billion per
volume) for 7 hours every day for their first three weeks of growth. Another set of seedlings grown
in clean air was fumigated in the same concentrations for only one 7-hour period after the first three
weeks of growth. The second set of seedlings demonstrated dead leaves and double the amounts of
stress ethylene produced by the first set. The results indicate that intermittent episodes of elevated
levels of atmospheric ozone may be more harmful to peas than constant high levels of ozone. The
study also found that the presence of additional pollutants such as nitrogen oxides significantly
enhances leaf injury by increasing stress ethylene production. (Wall and Strong, 1985).
It has been suggested that ozone is also a factor in the forest decline that has occurred in
central Europe and in California, perhaps in combination with other pollutants or other
environmental stresses. The evidence of decline is especially pronounced at higher altitudes where
ozone levels may be greater and more persistent. Most researchers say that a link is likely but
difficult to identify, so research is still being performed in this area. (Goldstein, 1997).
Regulation of Ozone and Its Interregional Transport
As mentioned previously, the EPA has regulated ozone for decades through the imposition of
maximum standards under the Clean Air Act. Under the Act, however, the individual states are
responsible for the implementation of the standards set by EPA. The states submit State
Implementation Plans (SIPs) which document how they will meet the standards by reducing
emissions of ozone precursors from sources such as cars, fuels, industrial facilities, power plants, and
consumer or commercial products. So far, state plans include controls on certain stationary sources,
development of cleaner cars and fuels, the use of special nozzles at the pumps of certain gas stations
to recapture gasoline vapors, and vehicle inspection programs.
States in the Northeast have struggled for decades to meet the standards for ozone in urban
areas, but have failed to attain the required levels. Because they are not in attainment, they have
been forced to implement more significant and costlier pollution reduction measures than other areas
of the country, except California. Despite these additional measures, however, they continue to
exceed standards for ozone and its precursors. The states in the Northeast claim that, unless
something is done to address the transport of ozone and other pollutants that cause ozone from other
states, attainment of the standards is impossible.
This long-range interstate flow of air pollution has been the subject of conflict between these
two regions for years. The frustration for the Northeast states has stemmed from the fact that those
sources in the pollution-generating states to the west are beyond their control. The Midwest, instead,
has claimed that the high ozone levels in the Northeast have been caused by local sources and that
the contribution of any transport was minimal. Given this inter-regional hostility, a cooperative
8
effort to address these issues seemed unlikely for many years.
In an effort to begin to deal with ozone transport within the Northeast Corridor, Congress
created the Ozone Transport Commission (OTC) with the passage of the 1990 Clean Air Act
Amendments (CAA, Section 7511c). Since that time, the OTC has adopted many regional pollution
control measures across the Ozone Transport Region, an area that encompasses Connecticut,
Delaware, the District of Columbia, Maine, Maryland, Massachusetts, New Hampshire, New Jersey,
New York, Pennsylvania, Rhode Island, Vermont and northern Virginia. The measures address
emissions of both hydrocarbons and nitrogen oxides from stationary and mobile sources, and include
the development of a regionwide mechanism for trading allowances for NOx emissions in
consultation with EPA. However, the region covered by the OTC still failed to encompass states
with pollution sources in upwind areas, particularly the Midwestern states which are home to coalfired power plants many believe are responsible for regional ozone formation and transport to the
Northeast. (OTC, 1998)
In 1995, the Ozone Transport Assessment Group (OTAG) was established, which was a
voluntary group of representatives from government, industry, environmental groups and others from
37 states. OTAG comprised the states in the Ozone Transport Region as well as most Midwestern
and Southern states. OTAG=s purpose was to determine the extent of the ozone transport problem
in the eastern part of the country and develop recommendations to the EPA to determine how to
address it. (OTC, 1998).
In June of 1997, after two years of study and periods of contentious debate, OTAG released
its report and recommendations to EPA. In the report, OTAG confirmed that the eastern half of the
United States was indeed experiencing pollution coming from elsewhere. In fact, through modeling
and monitoring data developed by OTAG workgroups, it was estimated that the range of ozone and
precursor transport is approximately 150 to over 500 miles. The extent of the transport, of course,
depends on a variety of meterological factors involving ozone and its precursors, including weather
systems, atmospheric stability and persistent wind patterns. OTAG=s modeling found that on days
when the Northeast typically experienced its most severe ozone days, the winds came at higher
speeds from the west and southwest. (NESCAUM, 1997) Based on its findings, OTAG
recommendations to the EPA to reduce regional transport included increased utility controls,
increased research, and an emission trading program for nitrous oxides similar to that established for
sulfur dioxide under the Acid Rain program. (LeClair, 1997).
In response to the OTAG recommendations, the EPA in September of this year issued a rule
requiring 22 states and the District of Columbia to submit SIPs that address the regional transport of
ozone through reductions of nitrogen oxides emissions. The rule calls for a reduction in emissions
by 28%, or 1.2 million tons, over the next several years. Although the EPA did not mandate which
sources must be targeted to reach the reduction levels, its plan demonstrated that the most costeffective approach will be the control of electric utilities, which are currently the largest contributors
and the least controlled sources. Most of these utilities are located in six states: Ohio, Indiana,
Illinois, West Virginia, Michigan and Pennsylvania. To minimize the estimated costs incurred, the
9
agency encouraged states to establish a pollution trading system for electric utilities similar to the
sulfur dioxide trading program. The reductions required by this rule must be in place by May 2003.
(EPA, 1998).
Reaction to the new rule was predictable. The Northeast governors hailed the new rule as a
victory for clean air in the Northeast and a much-awaited Aleveling of the playing field@ between
the regions. The Midwestern governors denounced the rule arguing that it was unnecessary, unjust
and unaffordable. It remains to be seen what the actual costs will be to implement this rule and the
extent of the benefits that will result.
Conclusion
It is apparent from the research performed to date that ozone presents a significant health
hazard. Despite regulatory efforts, the control of ozone remains complex because of its pervasiveness
and its nature as a secondary pollutant. However, these control efforts are on-going and hopefully
the recent tactics by the EPA, once implemented, will result in lower levels of ozone across the
country, bringing health benefits to millions living in affected areas.
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ENDNOTES
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10. Goldstein, A. (1997). Review, AForest Decline and Ozone: a Comparison of Controlled
Chamber and Field Experiments.@ Quarterly Review of Biology 12:489.
11. Jakab, G.J., Spannhake, E.W., Canning, B.J., Kleegerger, S.R., and Gilmour, M.I. (1995).
The Effects of Ozone on Immune Function. Environmental Health Perspectives 103: 7789.
12. Koenig, J.Q. (1995). Effect of Ozone on Respiratory Responses in Subjects with Asthma.
Environmental Health Perspectives 103: 103-105.
13. Korrick, S.A., Neas, L.M., Dockery, D.W., Gold, D.R., Allen, G.A., Hill, B.L., Kimball,
K.D., Rosner, B.A., and Speizer, F.E. (1998). Effects of Ozone and Other Pollutants on
the Pulmonary Function of Adult Hikers. Environmental Health Perspectives 106:93-99.
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15. LeClair, V. (1997). OTAG Recommends Ozone Controls Tailored to Pollution
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16. Leikauf, G.D., Simpson, L.G., Santrock, J., Zhao, Q., Abbinante-Nissen, J., Zhao, S., and
Driscoll, K.E. (1995). Airway Epithelial Cell Responses to Ozone Injury. Environmental
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17. Mehlhorn, H., and Wellburn, A.R. (1985). Stress Ethylene Formation Determines Plant
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19. Northeast States for Coordinated Air Use Management (NESCAUM) (1997). AThe
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Boston, MA.
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20. Office of Technology Assessment, United States Congress (1988). AUrban Ozone and
the Clean Air Act: Problems and Proposals for Change.@ Washington, D.C.
21. Ozone Transport Commission (1998). APollution Control Strategies in the Northeast and
Mid-Atlantic States to Clean Up Ground-Level Ozone: Progress to Date and A Look
Towards the Future.@ Washington, D.C.
22. Romieu, I., Meneses, F., and Ruiz, S. (1997). Effects of Intermittent ozone Exposure on
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Smog@ (R.F. Kosobud, W.A. Test and D.A. Hanson., eds.) pp. 121-131. Federal Reserve
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Ambient Ozone Levels and Emergency Department Visits for Asthma in Central New
Jersey. Environmental Health Perspectives 103: 97-102.
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N. (1995). Children at Risk From Ozone Air Pollution B United States, 1991-1993.
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